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However, excess ROS induces inflammatory cell infiltration and macrophage polarization through mitochondrial homeostasis disruption and production of pro-inflammatory factors, forming a vicious cycle of central nerve inflammation and ROS production, further aggravating inflammation and the formation of glial cell scar

Even more alarming are reports of HCC from NAFLD that occurred in the absence of cirrhosis[4]

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However, the reduction in contractility observed in the presence of tempol in the AG (44% reduction, compared to the absence) may be due to the conversion of O 2 into H 2 O 2 stimulated by this mimetic, thereby reducing the amount of O 2 and its availability for ONOO formation, which is produced through its reaction with NO , ultimately decreasing tracheal hyperresponsiveness

This could be as simple as a vitamin deficiency, or a complication of diabetes